Department of Regenerative Dermatology, Graduate School of Medicine, Osaka University, Osaka, Japan.
Exp Dermatol. 2013 Mar;22(3):168-71. doi: 10.1111/exd.12024. Epub 2012 Sep 28.
Androgens stimulate beard growth but suppress hair growth in androgenetic alopecia (AGA). This condition is known as 'androgen paradox'. Human pilosebaceous units possess enough enzymes to form the active androgens testosterone and dihydrotestosterone. In hair follicles, 5α-reductase type 1 and 2, androgen receptors (AR) and AR coactivators can regulate androgen sensitivity of dermal papillae (DP). To regulate hair growth, androgens stimulate production of IGF-1 as positive mediators from beard DP cells and of TGF-β1, TGF-β2, dickkopf1 and IL-6 as negative mediators from balding DP cells. In addition, androgens enhance inducible nitric oxide synthase from occipital DP cells and stem cell factor for positive regulation of hair growth in beard and negative regulation of balding DP cells. Moreover, AGA involves crosstalk between androgen and Wnt/β-catenin signalling. Finally, recent data on susceptibility genes have provided us with the impetus to investigate the molecular pathogenesis of AGA.
雄激素刺激胡须生长,但抑制雄性激素脱发(AGA)中的毛发生长。这种情况被称为“雄激素悖论”。人体的毳毛皮脂腺单位拥有足够的酶来形成活性雄激素睾酮和二氢睾酮。在毛囊中,5α-还原酶 1 型和 2 型、雄激素受体 (AR) 和 AR 共激活剂可以调节真皮乳头 (DP) 的雄激素敏感性。为了调节头发生长,雄激素刺激 IGF-1 的产生,作为胡须 DP 细胞的正向调节剂,以及 TGF-β1、TGF-β2、dickkopf1 和 IL-6 作为脱发 DP 细胞的负向调节剂。此外,雄激素增强枕部 DP 细胞中的诱导型一氧化氮合酶和干细胞因子,对头发生长具有正向调节作用(胡须)和负向调节脱发 DP 细胞。此外,AGA 涉及雄激素和 Wnt/β-连环蛋白信号之间的串扰。最后,关于易感基因的最新数据为我们研究 AGA 的分子发病机制提供了动力。